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Passive smoking and risk of coronary heartdisease and stroke: prospective study with cotinine measurement
Peter H Whincup, Julie A Gilg, Jonathan R Emberson, Martin J Jarvis, ColinFeyerabend, Andrew Bryant, Mary Walker and Derek G Cook
2004;329;200-205; originally published online 30 Jun 2004;
BMJdoi:10.1136/bmj.38146.427188.55
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We thank the many people who supported the conduct of this
(Prepared for the Gulf War Illness Advisory Committee, Department of
study: representatives of the armed services; the British Legion,
National Defence, by Goss Gilroy Inc. Management Consultants.)
in particular Terry English; National Gulf Veterans and Families
www.dnd.ca/site/reports/Health/vol1_TOC_e.htm (accessed 10 May2004).
Association; Gulf Veterans Association; and, most importantly,
Ishoy T, Andersson AM, Suadicani P, Guldager B, Appleyard M. Major
the study participants for the time and effort involved. We also
reproductive health characteristics in male Gulf veterans. Dan Med Bull
acknowledge the skills and commitment of those who worked
on the study, particularly Tommy Clarke, Graham Davies,
Kang H, Magee C, Mahan C, Lee K, Murphy F, Jackson L, et al. Pregnancy
Haydon Hughes, Juliet Jain, Sam Lewis, Margo Pelerin, Susan
outcomes among U.S. Gulf veterans: a population-based survey of 30,000veterans. Ann Epidemiol 2001;11:504-11.
Prior, Darren Reed, Patrick Sampson, and Janet Sullivan. For
Araneta MR, Schlangen KM, Edmonds LD, Destiche DA, Merz RD,
supplying cohort data and for invaluable help with queries, we
Hobbs CA, et al. Prevalence of birth defects among infants of Gulf veter-
thank all members of the Gulf Veterans Illness Unit (now the
ans in Arkansas, Arizona, California, Georgia, Hawaii, and Iowa,
Veterans Policy Unit) at the Ministry of Defence, in particular
1989-1993. Birth Defects Res Part A Clin Mol Teratol 2003;67:246-60.
Nick Blatchley, John Graham, Philip Bolton, Linda Walpole, and
Sim M, Abramson M, Forbes A, Glass D, Ikin J, Ittak P, et al. Australian Gulfveterans’ health study 2003. Vol 2. Commonwealth Department of
Chris Baker. We also thank Steve McManus and colleagues at
Veterans’ Affairs, 2003. www.dva.gov.au/media/publicat/2003/gulfwarhs
the British Forces Post Office for providing valuable
information on serving status and addresses.
Doyle P, Maconochie N, Davies G, Maconochie I, Pelerin M, Prior S, et al.Miscarriage, stillbirth and congenital malformation in the offspring of
UK veterans of the first Gulf war. Int J Epidemiol 2004;33:74-86.
Funding: The study was funded by the UK Ministry of Defence
10 Maconochie N, Doyle P, Davies G, Lewis S, Pelerin M, Prior S, et al. The
and administered by the UK Medical Research Council.
study of reproductive outcome and the health of offspring of UKveterans of the Gulf war: methods and description of the study
population. BMC Public Health 2003;3:4.
Ethical approval: West Midlands multi-centre research ethics
11 World Health Organization. WHO laboratory manual for the examination of
committee; London School of Hygiene and Tropical Medicine
human semen and sperm-cervical mucus interaction. 3rd ed. Cambridge, UK:Cambridge University Press on behalf of WHO, 1992.
12 Breslow NE, Day NE. Statistical methods in cancer research. Vol II. Theanalysis of cohort studies. Lyon: International Agency for Research on
Penman AD, Currier MM, Tarver RS. No evidence of increase in birth
defects and health problems among children born to Persian Gulf veter-
13 Abou-Donia MB, Suliman HB, Khan WA, Abdel-Rahman AA. Testicular
ans in Mississippi. Mil Med 1996;161:1-6.
germ-cell apoptosis in stressed rats following combined exposure to
Cowan DN, DeFraites RF, Gray GC, Goldenbaum MB, Wishik SM. The
pyridostigmine bromide, N-diethyl m-toluamide (DEET) and permeth-
risk of birth defects among children of Persian Gulf veterans. N Engl J
rin. J Toxicol Environ Health A. 2003;66:57-73.
14 Military Health Research Advisory Group (MHRAG). MRC review of
Araneta MRG, Moore CA, Olney RS, Edmonds LD, Karcher JA,
research into UK Gulf veterans’ illnesses 2003. London: Medical Research
McDonough C, et al. Goldenhar syndrome among infants born in
Council, 2003. www.mrc.ac.uk/pdf-gulf-illness-review.pdf (10 May 2004).
military hospitals to Gulf veterans. Teratology 1997;56:244-51.Health study of Canadian forces personnel involved in the 1991 conflict in thePersian Gulf. Vol 1. Canadian Department of National Defence, 1998.Passive smoking and risk of coronary heart disease andstroke: prospective study with cotinine measurementPeter H Whincup, Julie A Gilg, Jonathan R Emberson, Martin J Jarvis, Colin Feyerabend,Andrew Bryant, Mary Walker, Derek G CookAbstract
Hazard ratios (for cotinine 0.8-14.0 v ≤ 0.7 ng/ml)
were particularly increased during the first (3.73, 1.32
Objective To examine the associations between a
to 10.58) and second five year follow up periods (1.95,
biomarker of overall passive exposure to tobacco
1.09 to 3.48) compared with later periods. There was
smoke (serum cotinine concentration) and risk of
no consistent association between cotinine
Design Prospective population based study in generalConclusion Studies based on reports of smoking in a
practice (the British regional heart study).
partner alone seem to underestimate the risks of
Participants 4729 men in 18 towns who provided
exposure to passive smoking. Further prospective
baseline blood samples (for cotinine assay) and a
studies relating biomarkers of passive smoking to risk
detailed smoking history in 1978-80.
of coronary heart disease are needed.Main outcome measure Major coronary heart
disease and stroke events (fatal and non-fatal) during20 years of follow up.IntroductionResults 2105 men who said they did not smoke and
Meta-analyses examining the effect of living with a
who had cotinine concentrations < 14.1 ng/ml were
cigarette smoker on risk of coronary heart disease
divided into four equal sized groups on the basis of
(CHD) among non-smokers have shown an overall
cotinine concentrations. Relative hazards (95%
increase in risk of about one quarter, after adjustment
confidence intervals) for coronary heart disease in the
for potential confounding factors.1 2 Passive smoking
second (0.8-1.4 ng/ml), third (1.5-2.7 ng/ml), and
fourth (2.8-14.0 ng/ml) quarters of cotinineconcentration compared with the first ( ≤ 0.7 ng/ml)were 1.45 (1.01 to 2.08), 1.49 (1.03 to 2.14), and 1.57
This is the abridged version of an article that was posted on
(1.08 to 2.28), respectively, after adjustment for
bmj.com on 30 June 2004: http://bmj.com/cgi/doi/10.1136/
established risk factors for coronary heart disease.BMJ VOLUME 329 24 JULY 2004
Living with someone who smokes accounts for less
than half of the variation in cotinine concentration
among non-smokers4 and does not take account of
additional exposure in workplaces and in public places
(particularly pubs and restaurants).5 Biomarkers of
passive exposure to smoking, particularly cotinine (a
nicotine metabolite), can provide a summary measure of
exposure from all these sources.6 Although cotinine
concentration in non-smokers has been strongly related
to prevalent CHD,7 there are no published reports of the
prospective associations between serum cotinine con-
centration and risk of CHD and stroke in non-smokers.
0-0.9 1-1.9 2-2.9 3-3.9 4-4.9 5-5.9 6-6.9 7-7.9 8-8.9 9-9.9
We examined these associations in the British regional
heart study, a prospective study of cardiovascular disease
in middle aged men, using retained baseline samples for
Fig 1 Distribution of serum cotinine concentrations among current
non-smokers; lifelong non-smokers and former smokers are shown
retrospective measurement of cotinine.
Epidemiology andPublic Health, RoyalFree and University
reviews of patients’ records every two years throughout
The British regional heart study is a prospective study
follow up.8 The analyses presented are based on all first
of cardiovascular disease in 7735 men aged 40-59
major CHD or stroke events during the follow up
Martin J Jarvisprofessor of health
period to December 2000, with an average follow up of
Baseline assessment—In 1978-80, research nurses
18.5 years for men who had no myocardial infarction
administered a questionnaire on present and previous
smoking habits (cigarettes, cigar, pipe), alcohol intake,
Definition of baseline smoking status—Men were
physical activity, and medical history (including angina,
classified as “current non-smokers” at baseline if they
myocardial infarction, stroke, and diabetes diagnosed
reported that they did not smoke cigarettes, cigars, or a
by a doctor). Participants also completed a question-
pipe and had a serum cotinine concentration < 14.1
naire on chest pain. Blood pressure, non-fasting total
ng/ml.10 Among these men, “lifelong non-smokers”
serum cholesterol concentration, and high density
were those who reported never having smoked
lipoprotein (HDL) cholesterol were measured. Serum
cigarettes, cigars, or a pipe. For comparison purposes,
samples were placed in long term storage at − 20°C in
“light active smokers” were men who reported
the last 18 study towns. In 2001-2, these were thawed
smoking 1-9 cigarettes a day, irrespective of cotinine
Follow up—All men were followed up for all cause
Statistical methods—We used Cox proportional haz-
mortality and cardiovascular morbidity. Deaths were
ards models, stratified by town of residence, to examine
flagged by the NHS central registers. We obtained
the independent contribution of serum cotinine
information on non-fatal CHD events and strokes
concentration to the risks of CHD and stroke. These
from general practitioners’ reports, and from regular
produced relative hazards, adjusted for age and other
Hazard ratios for cotinine group and risk of coronary heart disease (CHD) over 20 years of follow up
Cotinine concentration (ng/ml)2.8-14.0Active smokers (1-9/day)P value for trend*Excluding former smokers
*From tests for linear trend between log (cotinine) concentration and CHD hazard across passive smoking groups.†For CHD: adjustment 1 stratified by town and adjusted for age; adjustment 2 additionally adjusted for systolic blood pressure, diastolic blood pressure, total cholesterol, HDL cholesterol, FEV ,
height, and pre-existing CHD; adjustment 3 additionally adjusted for BMI, triglycerides, white cell count, diabetes, physical activity (none, occasional, light, moderate or more), alcohol intake(none/occasional, light/moderate, heavy), and social class (I, II, III non-manual, III manual, IV, V, and Armed Forces).BMJ VOLUME 329 24 JULY 2004
risk factors, for each quarter of the distribution ofserum cotinine concentration compared with the
lowest. We carried out overall tests of the association,
fitting the continuous relation between log cotinine
concentration and risk of CHD (see bmj.com). Wefitted age, body mass index, height, systolic blood pres-
sure, diastolic blood pressure, serum total cholesterol,high density lipoprotein cholesterol, white cell count,
lung function (forced expiratory volume in one second
(FEV )), and triglyceride concentration as continuous
variables. Physical activity was fitted as a factor with
four levels, alcohol intake with three levels, and social
class with seven levels. History of cigarette smoking,pre-existing CHD, and diabetes were fitted as dichoto-
Fig 2 Proportion of men with major CHD by years of follow up in
each smoking group. “Light passive” refers to lowest quarter ofcotinine concentration among non-smokers (0-0.7 ng/ml), “heavypassive” to upper three quarters of cotinine concentration combined
(0.8 to 14.0 ng/ml), “light active” to men smoking 1-9 cigarettes aday
In the last 18 towns of the study, 5661 men took part(78% response rate). For 4729 of these we had data onhistory of smoking and blood samples for cotinine
Influence of follow up period—In a Kaplan-Meier plot
analysis. These men resembled the whole study popu-
showing the cumulative proportions of men with
lation in reported smoking habits and risks of CHD
major CHD over time among three groups (light pas-
and stroke. A total of 2158 men reported that they
sive (lowest cotinine quarter), heavy passive (upper
were current non-smokers, of whom 2105 (97.5%) had
three cotinine quarters), and light active (1-9
serum cotinine concentrations < 14.1 ng/ml. Of these,
cigarettes/day)) we found that the heavy passive and
945 men were classified as lifelong non-smokers, the
light active groups diverged rapidly from the light pas-
remaining 1160 as former smokers. The cotinine
sive group during the first years of follow up but
distributions of these two groups (fig 1) were skewed,
remained almost parallel during later years (fig 2). The
with a slightly higher geometric mean cotinine among
corresponding hazard ratios for cotinine and risk of
former smokers than among lifelong non-smokers
CHD in separate five year follow up periods were high-
(1.49 v 1.18 ng/ml). Few men in either group had coti-
est in the early years of follow up and declined with
nine concentrations close to the 14.1 ng/ml cut off.
increasing duration of follow up (bmj.com). These pat-
Serum cotinine and cardiovascular risk factors—
terns were little affected by adjustment for cardiovascu-
Among current non-smokers, cotinine concentrations
lar risk factors, and again the hazard ratios for the
were not consistently related to age, total cholesterol
heavier passive smoking groups were comparable with
concentration, physical activity score, or prevalent
those of light active smokers. Restriction of these
CHD but showed graded positive associations with
analyses to lifelong non-smokers or to men with no
mean body mass index, systolic and diastolic blood
evidence of pre-existing CHD had no material effect
pressure, high density lipoprotein cholesterol, white
cell count, and triglycerides (weakly) and positive asso-
Serum cotinine exposure and stroke—There was no
ciations with the prevalence of former smoking, heavy
strong association between cotinine concentration and
drinking, and manual occupation. Cotinine concentra-
stroke among non-smokers, either before or after
tions were inversely associated with FEV , prevalence
adjustment for major cardiovascular risk factors (see
of low alcohol intake, and residence in southern
bmj.com). Analyses based on lifelong non-smokers
England. These associations were generally little
affected when we excluded former smokers. Lightactive smokers had lower mean body mass index,
Discussion
diastolic blood pressure, and FEV and a higher mean
white cell count than men who did not smoke.
We believe this is the first published report to relate
Serum cotinine concentration and CHD risk—We
passive exposure to smoking, based on cotinine meas-
examined the association between quarters of the coti-
urements, prospectively to the risks of CHD and stroke,
nine distribution and CHD hazard ratios among all
although cotinine concentration among non-smokers
2105 current non-smokers using the complete follow
has been related to prevalence of CHD.7 Our study was
up period (table). The risks in the upper three cotinine
conducted in a geographically and socially representa-
groups were markedly higher than the risk in the
tive sample of middle aged men.8 We were able to
lowest group, with a relative hazard of 1.61 in the
adjust for a wide range of potential confounding vari-
highest group in the simplest model, a hazard estimate
ables, and this had little effect on the results, in agree-
similar to that of light active smokers. The association
ment with earlier reports.1 2 A greater concern is the
between cotinine concentration and CHD seemed
possibility that men in the higher cotinine groups were
graded and was not markedly affected by adjustment
smoking cigarettes on an intermittent basis. However,
for other cardiovascular risk factors. When we
study participants had no incentive to provide inaccu-
examined the overall association between cotinine
rate information, there was close agreement between
concentration and CHD, we found that a doubling of
reported smoking and cotinine concentration, and the
cotinine concentration was associated with a hazard
increase of 16% (95% confidence interval 6% to 27%).
approached, even among former smokers. In addition,
BMJ VOLUME 329 24 JULY 2004
almost all surviving current non-smokers (99%) contin-
What is already known on this topic
ued to report that they were non-smokers in responsesto postal questionnaires five and 12 years later.
Passive smoking (generally defined as living with
Passive smoking and CHD
someone who smokes) is associated with an
Although the study was modest in size with limited
increase in risk of coronary heart disease risk of
precision, our results suggest that the relative risk of
CHD associated with high levels of passive exposure to
Passive smoking may also increase the risk of
smoke is greater than that estimated for partner smok-
ing alone, even at exposure levels of 20 cigarettes a dayor more.2 The similarity of relative risks among partici-
Living with someone who smokes is not the only
pants with substantial exposure to passive smoking
relevant source of passive smoking, but few studies
and those who were light active smokers exposure is
have taken account of all sources of exposure by
consistent with earlier findings.1 The high relative risk
relating biomarkers such as cotinine to disease
associated with exposure to passive smoking in our
study probably reflects the wide range of cotinine con-centrations observed among non-smokers; the average
What this study adds
concentrations of the lowest and highest cotinine
Higher concentrations of serum cotinine among
quarters differed by almost 10-fold. This range seems
non-smokers are associated with an excess risk of
considerably wider than that which might be expected
coronary heart disease of about 50-60%, but show
from partner smoking alone, which in recent data has
been associated with average increases in cotinine con-centration of about 3.6-fold.4 A 3.6 fold difference in
Risks associated with passive smoking are
cotinine concentration would, on the basis of the log
widespread among non-smokers in this study
cotinine-CHD association defined in the present study,
be associated with a relative risk of CHD of about 1.32(95% confidence interval 1.12 to 1.55)—a figure similar
to the estimates of the effect of a partner smoking
concentration and coronary heart disease seems
obtained in the earlier systematic reviews.1 2
to decline with time since assessment of exposure,
The marked attenuation in the relative risks
suggesting that studies examining the association
relating cotinine and CHD with increasing duration of
of passive smoking to coronary heart disease over
follow up suggests that a single measurement of
long follow up periods may have underestimated
cotinine is a weak measure of the long term effects of
passive smoking. In the present study population, ahigh initial cotinine concentration probably provides asystematic overestimate of the true longer term passiveexposure to smoke, which has declined markedly in
sive exposure to tobacco smoke and risk of stroke sug-
Britain during the follow up period—partly because of
gests that the association between passive smoking and
a declining prevalence of active smoking11 and partly
CHD is specific and is not simply due to selection bias
because passive exposure to smoke in public places
placing high risk participants in the higher cotinine
and work places has declined.12 In studies with a single
assessment of exposure, analyses based on the first
Conclusion
decade or so of follow up may well provide a better
High overall exposure to passive smoking seems to be
indication of true relative risks than those based on
associated with a greater excess risk of CHD than part-
ner smoking and is widespread in non-smokers,
As well as providing evidence that the relative risks
suggesting that the effects of passive smoking may have
associated with overall passive exposure to tobacco
been underestimated in earlier studies. Our results add
smoke are higher than those associated with partner
to the weight of evidence suggesting that exposure to
smoking alone, the results indicate that important
passive smoking is a public health hazard and should
degrees of exposure to passive smoke were widespread
in the present cohort, in which three quarters of non-smokers had an increased risk of CHD associated with
increased exposure to cotinine. In contrast, the
Funding: The analysis of cotinine measurements was supported
prevalences of partner smoking in studies of
by a Project Grant from the BUPA Foundation. The British
non-smoking men in earlier reports have often been
regional heart study is funded by the British Heart Foundationand the Department of Health.
well below 50%.13 14 Taken in combination with the
higher estimated relative risks, the high prevalence of
Ethical approval: Ethical approval was provided by the Medical
exposure suggests that the contribution of passive
Research Council and subsequently by the relevant local and
smoking to the population attributable risk of CHD
multicentre research ethics committees.Passive smoking and stroke
Law MR, Morris JK, Wald NJ. Environmental tobacco smoke exposureand ischaemic heart disease: an evaluation of the evidence. BMJ
Our results do not support the earlier suggestion from
a retrospective case-control study that passive tobacco
He J, Vupputuri S, Allen K, Prerost MR, Hughes J, Whelton PK. Passivesmoking and the risk of coronary heart disease—a meta-analysis of
smoke exposure increases risk of stroke,3 though the
epidemiologic studies. N Engl J Med 1999;340:920-6.
confidence intervals around the hazard estimates are
Bonita R, Duncan J, Truelsen T, Jackson RT, Beaglehole R. Passive smok-ing as well as active smoking increases the risk of acute stroke. Tob Control
wide. The lack of an apparent association between pas-
BMJ VOLUME 329 24 JULY 2004
Jarvis MJ, Feyerabend C, Bryant A, Hedges B, Primatesta P. Passive smok-
10 Jarvis MJ, Tunstall-Pedoe H, Feyerabend C, Vesey C, Saloojee Y.
ing in the home: plasma cotinine concentrations in non-smokers with
Comparison of tests used to distinguish smokers from nonsmokers. Am J
smoking partners. Tob Control 2001;10:368-74.Public Health 1987;77:1435-8.
Jarvis MJ, Foulds J, Feyerabend C. Exposure to passive smoking among
11 Jarvis MJ, Goddard E, Higgins V, Feyerabend C, Bryant A, Cook DG.
bar staff. Br J Addict 1992;87:111-3.
Children’s exposure to passive smoking in England since the 1980s: coti-
Jarvis M, Tunstall-Pedoe H, Feyerabend C, Vesey C, Salloojee Y.
nine evidence from population surveys. BMJ 2000;321:343-5.
Biochemical markers of smoke absorption and self reported exposure to
12 Walker A, O’Brien M, Traynor J, Fox K, Goddard E, Foster K. Living in
passive smoking. J Epidemiol Community Health 1984;38:335-9.Britain: results from the 2001 general household survey. London: Stationery
Tunstall-Pedoe H, Brown CA, Woodward M, Tavendale R. Passive smok-
ing by self report and serum cotinine and the prevalence of respiratory
13 Sandler DP, Comstock GW, Helsing KJ, Shore DL. Deaths from all causes
and coronary heart disease in the Scottish heart health study. J Epidemiol
in non-smokers who lived with smokers. Am J Public HealthCommunity Health 1995;49:139-43.
Walker M, Shaper AG, Lennon L, Whincup PH. Twenty year follow-up of
14 Hole DJ, Gillis CR, Chopra C, Hawthorne VM. Passive smoking and car-
a cohort based in general practices in 24 British towns. J Public Health Med
diorespiratory health in a general population in the west of Scotland. BMJ
Feyerabend C, Russell MA. A rapid gas-liquid chromatographic method
for the determination of cotinine and nicotine in biological fluids. JPharm Pharmacol 1990;42:450-2.Acquisition of Helicobacter pylori infection after outbreaks ofgastroenteritis: prospective cohort survey in institutionalisedyoung peopleRémi Laporte, Philippe Pernes, Pascale Pronni, Frédéric Gottrand, Pascal Vincent
The exact mode of spread of Helicobacter pylori is still
detected by using the non-invasive HpSA stool
unknown. Transmission during transit disorders of the
antigen test (Meridian; 91% sensitivity and 93%
gastrointestinal tract has been suggested, although
specificity).4 Stool samples were stored and trans-
there is no evidence to date of transmission during
ported at 4°C within 48 hours and then frozen. The
outbreaks of gastroenteritis.1–3 We determined whether
residents were monitored for one year. Events and
gastroenteritis in young people infected with H pylori
clinical data were recorded daily by nurses. Gastroen-
can lead to acquisition of the bacterium by peers.
teritis was defined as a sudden outbreak of liquidstools in more than two residents concurrently. For
Centre Antoine deSaint-Exupéry,Vendin-le-Vieil,
Participants, methods, and results
each patient with H pylori infection, we defined oneday of potentially infective diarrhoea or vomiting as
Our study took place in a French institution for
that when at least one liquid stool or vomitus was
neurologically handicapped children and adolescents.
emitted. Stool samples were collected every week for
The young people had been institutionalised for
each resident who was free of infection at the study
several years and resided across five housing sections
outset, and at the end of the study we compared the
(A to E). We included all 112 residents in May 2001. H
last sample with the first sample. When conversion
pylori infection present at the outset of the study was
was observed, we identified the oldest positive
stool sample collected from that patient during follow
Person days of infective diarrhoea per week
The prevalence of H pylori infection was high; 47
Diarrhoea outbreak level limit (95% limit Poisson distribution)
of the 112 residents (42%) were positive for H pylori at
Person days of infective vomitus per week
the study outset. Seven of the 65 residents who were
initially negative for H pylori showed conversion
Individual living in another section but in close contact with
during follow up (figure). Five of the seven young peo-
ple lived in section E, and our records showed that the
two other residents had frequent contacts with the
infected patients from section E during physiotherapy
and entertainment sessions. Vomitus was rare in all
sections. The frequency of diarrhoeal stools from the
infected patients varied across sections; residents of
sections A and B had 475 and 338 person days of
potentially infective diarrhoea over the year, respec-tively. Acute diarrhoea was rare in these sections, and
no outbreaks of gastroenteritis were recorded. A lower
May Jun Jul Aug Sep Oct Nov Dec Jan Feb Mar Apr May
frequency of diarrhoeal stools was observed in
sections C, D, and E; 34, 104, and 164 person days ofpotentially infective diarrhoea over the year, respec-
Relation between new cases of Helicobacter pylori infection andexposure to infective diarrhoea and vomitus in housing section E
tively. The frequency was always low in sections C andD, where no outbreaks of gastroenteritis were
BMJ VOLUME 329 24 JULY 2004

Activation of sperm motility in striped bass viaShuyang HeKaren Jenkins-KeeranL. Curry Woods IIIaDepartment of Animal and Avian Sciences, University of Maryland,bNational Institutes of Health, Bethesda, MD 20892, USAReceived 12 March 2003; accepted 26 August 2003The objective of the present study was to identify the effect of osmolality, ions (Kþ, Hþ, Ca2þ,Mg2þ) and cAMP on the ini